Why do the lungs age faster in COPD and how can we slow it down?

Chronic obstructive pulmonary disease (COPD) is a long-term lung condition that happens when your lungs become inflamed and damaged and your airways narrow. This makes it harder for air to move in and out of your lungs so you become breathless. 

COPD is a progressive condition which means it gets worse over time. We have treatments to help improve people’s symptoms, but there are currently very few options for slowing progression, and nothing to stop it.

What happens to cells in our body when we age?

All of us age, but we know that the lungs of people with COPD age faster than those of people whose lungs are healthy. As we get older, some of our cells enter a state called "senescence". These senescent cells are still alive, but they no longer work properly. Instead of helping repair damaged tissue as they should, they release substances that can cause inflammation and further damage. In COPD, these cells are found in higher numbers and may contribute to how the condition progresses. 

How do our cells communicate with each other?

Cells can communicate with each other by releasing tiny particles called extracellular vesicles (EVs). These act like small packages and carry biological messages between cells. Previous research has shown that lung lining cells (called epithelial cells) from people with COPD release ‘packages’ containing molecules that can encourage healthy cells to become senescent too. This suggests that EVs may help spread ageing and damage throughout the lungs. 

How does this affect progression of COPD?

We’re trying to understand whether EVs released by different types of lung cells also contribute to faster ageing in COPD. We’re comparing EVs produced by healthy lungs and the lungs of people with COPD, examining the messages they carry, and identifying which lung cells respond to them. We’re also investigating whether EVs from the lungs of people with COPD can trigger signs of ageing in healthy lung tissue. To do this, we’re using small slices of donated lung tissue that closely resemble the structure and cell types found in living lungs. By studying EVs in this more realistic way, we hope to better understand how ageing spreads within the lungs. 

How can understanding this help us treat COPD?

We all experience ageing. As a researcher, I am passionate about identifying the fundamental mechanisms that explain why some people develop age-related diseases while others do not. In COPD, the ageing process appears to happen much faster in the lungs. By understanding why this occurs, we hope to develop treatments that can protect lung function and improve the quality of life of millions of people affected by COPD and other age-related diseases including pulmonary fibrosis, cystic fibrosis, pulmonary hypertension, diabetes, and severe asthma. 

By identifying new mechanisms that drive lung ageing, the project could help pharmaceutical companies and researchers develop new drugs or therapies to slow, stop or even reverse some of the damage caused by COPD.